Measurement Model and Precision Analysis of Accelerometers for Maglev Vibration Isolation Platforms

High precision measurement of acceleration levels is required to allow active control for vibration isolation platforms. It is necessary to propose an accelerometer configuration measurement model that yields such a high measuring precision. In this paper, an accelerometer configuration to improve measurement accuracy is proposed. The corresponding calculation formulas of the angular acceleration were derived through theoretical analysis. A method is presented to minimize angular acceleration noise based on analysis of the root mean square noise of the angular acceleration. Moreover, the influence of installation position errors and accelerometer orientation errors on the calculation precision of the angular acceleration is studied. Comparisons of the output differences between the proposed configuration and the previous planar triangle configuration under the same installation errors are conducted by simulation. The simulation results show that installation errors have a relatively small impact on the calculation accuracy of the proposed configuration. To further verify the high calculation precision of the proposed configuration, experiments are carried out for both the proposed configuration and the planar triangle configuration. On the basis of the results of simulations and experiments, it can be concluded that the proposed configuration has higher angular acceleration calculation precision and can be applied to different platforms

Chronic morphine administration enhances nociceptive sensitivity and local cytokine production after incision

Abstract Background - The chronic use of opioids prior to surgery leads to lowered pain thresholds and exaggerated pain levels after these procedures. Several mechanisms have been proposed to explain this heightened sensitivity commonly termed opioid-induced hyperalgesia (OIH). Most of these proposed mechanisms involve plastic events in the central or peripheral nervous systems. Alterations in the abundance of peripheral mediators of nociception have not previously been explored. Results - In these experiments mice were treated with saline (control) or ascending daily doses of morphine to generate a state of OIH followed by hind paw incision. In other experiments morphine treatment was initiated at the time of incision. Both mechanical allodynia and peri-incisional skin cytokine levels were measured. Myeloperoxidase (MPO) assays were used to determine neutrophil activity near the wounds. The cytokine production inhibitor pentoxifylline was used to determine the functional significance of the excess cytokines in previously morphine treated animals. Mice treated chronically treated with morphine prior to incision were found to have enhanced skin levels of IL-1β, IL-6, G-CSF, KC and TNFα after incision at one or more time points compared to saline pretreated controls. The time courses of individual cytokines followed different patterns. There was no discernable effect of chronic morphine treatment on wound area neutrophil infiltration. Pentoxifylline reduced cytokine levels and reversed the excess mechanical sensitization caused by chronic morphine administration prior to incision. Morphine treatment initiated at the time of incision did not lead to a generalized enhancement of cytokine production or nociceptive sensitization in excess of the levels observed after incision alone. Conclusion - The enhanced level of nociceptive sensitization seen after incision in animals chronically exposed to morphine is associated with elevated levels of several cytokines previously reported to be relevant to this incisional pain model. The cytokines may be functional in supporting nociceptive sensitization because pentoxifylline reverses both peri-incisional skin cytokine levels and OIH. Opioid administration beginning at the time of incision does not seem to have the same cytokine enhancing effect. Approaches to postoperative pain control involving a reduction of cytokines may be an effective way to control excessive pain in patients chronically using opioids prior to surgical procedures.</p

DNA Methylation Modulates Nociceptive Sensitization after Incision.

DNA methylation is a key epigenetic mechanism controlling DNA accessibility and gene expression. Blockade of DNA methylation can significantly affect pain behaviors implicated in neuropathic and inflammatory pain. However, the role of DNA methylation with regard to postoperative pain has not yet been explored. In this study we sought to investigate the role of DNA methylation in modulating incisional pain and identify possible targets under DNA methylation and contributing to incisional pain. DNA methyltranferase (DNMT) inhibitor 5-Aza-2'-deoxycytidine significantly reduced incision-induced mechanical allodynia and thermal sensitivity. Aza-2'-deoxycytidine also reduced hindpaw swelling after incision, suggesting an anti-inflammatory effect. Global DNA methylation and DNMT3b expression were increased in skin after incision, but none of DNMT1, DNMT3a or DNMT3b was altered in spinal cord or DRG. The expression of proopiomelanocortin Pomc encoding β-endorphin and Oprm1 encoding the mu-opioid receptor were upregulated peripherally after incision; moreover, Oprm1 expression was further increased under DNMT inhibitor treatment. Finally, local peripheral injection of the opioid receptor antagonist naloxone significantly exacerbated incision-induced mechanical hypersensitivity. These results suggest that DNA methylation is functionally relevant to incisional nociceptive sensitization, and that mu-opioid receptor signaling might be one methylation regulated pathway controlling sensitization after incision

Conservation of genome content and virulence determinants among clinical and environmental isolates of Pseudomonas aeruginosa

Pseudomonas aeruginosa is a ubiquitous environmental bacterium capable of causing a variety of life-threatening human infections. The genetic basis for preferential infection of certain immunocompromised patients or individuals with cystic fibrosis by P. aeruginosa is not understood. To establish whether variation in the genomic repertoire of P. aeruginosa strains can be associated with a particular type of infection, we used a whole-genome DNA microarray to determine the genome content of 18 strains isolated from the most common human infections and environmental sources. A remarkable conservation of genes including those encoding nearly all known virulence factors was observed. Phylogenetic analysis of strain-specific genes revealed no correlation between genome content and infection type. Clusters of strain-specific genes in the P. aeruginosa genome, termed variable segments, appear to be preferential sites for the integration of novel genetic material. A specialized cloning vector was developed for capture and analysis of these genomic segments. With this capture system a site associated with the strain-specific ExoU cytotoxin-encoding gene was interrogated and an 80-kb genomic island carrying exoU was identified. These studies demonstrate that P. aeruginosa strains possess a highly conserved genome that encodes genes important for survival in numerous environments and allows it to cause a variety of human infections. The acquisition of novel genetic material, such as the exoU genomic island, through horizontal gene transfer may enhance colonization and survival in different host environments

In these experiments mice were subjected to nociceptive testing of the hind paw to establish the baseline threshold

Mice were then pre-treated with either saline or morphine for 4 days prior to hind paw incisions being made. After incision, groups of mice were treated daily with daily intraperitoneal saline or pentoxifylline as described in Methods. Nociceptive testing 72 hours after hind paw incision (2 hours after the last dose of pentoxifylline). **p < 0.01, N = 8/group.<p><b>Copyright information:</b></p><p>Taken from "Chronic morphine administration enhances nociceptive sensitivity and local cytokine production after incision"</p><p>http://www.molecularpain.com/content/4/1/7</p><p>Molecular Pain 2008;4():7-7.</p><p>Published online 22 Feb 2008</p><p>PMCID:PMC2279109.</p><p></p

Assessment of DNMT inhibitor 5-Aza-2′-deoxycytidine on incision-induced mechanical and thermal sensitization.

<p>Blocking DNMT attenuated incision-induced mechanical hypersensitivity (A) and thermal sensitization (B). Animals received intraperitoneal injection of 5-Aza-2′-deoxycytidine (4 mg/kg) or vehicle (saline) 24h and 2h prior to incision and once daily for 3 days after incision. Values are displayed as the mean ± SEM. N = 8. **p<0.01, 5-AZA-CdR + INC group vs. Veh + INC group. Veh = vehicle; INC = incision; 5-AZA-CdR = 5-Aza-2′-deoxycytidine.</p

Panel A displays the mechanical thresholds of mice in four different treatment groups: saline pretreatment/no incision, saline pretreatment/incision, morphine pretreatment/no incision, morphine pretreatment/incision

The values labeled pre-incision represent the nociceptive thresholds measured after 4 days of saline or morphine treatment but prior to hind paw incision. In panel B data are presented representing mechanical nociceptive thresholds in mice undergoing saline or morphine treatment beginning at the time of incision. Nociceptive thresholds were measured immediately before that day's dose of morphine. The statistical analysis presented reflects the results of two-way ANOVA comparing saline/incision values to morphine/incision ones. *p < 0.05, **p < 0.01, N = 6/group.<p><b>Copyright information:</b></p><p>Taken from "Chronic morphine administration enhances nociceptive sensitivity and local cytokine production after incision"</p><p>http://www.molecularpain.com/content/4/1/7</p><p>Molecular Pain 2008;4():7-7.</p><p>Published online 22 Feb 2008</p><p>PMCID:PMC2279109.</p><p></p